| dc.description.abstract | In holoendemic Plasmodium falciparum transmission areas such as western Kenya, severe malarial anemia [SMA,
hemoglobin (Hb) < 6.0 g/dL, with any density parasitemia] is the most common clinical manifestation of severe malaria
resulting in high rates of pediatric morbidity and mortality in these regions. Previous studies associated interleukin (IL)-13
with pathogenesis of different infectious diseases, including P. falciparum malaria. However, the functional roles of
polymorphic variants within the IL-13 promoter in conditioning susceptibility to SMA remain largely unexplored. As such,
the association between the IL-13 variants -7402 T/G (rs7719175) and -4729G/A (rs3091307) and susceptibility to SMA was
determined in children (n = 387) presenting with clinical symptoms of falciparum malaria and resident in a holoendemic
transmission region in western Kenya. Our results indicated no difference in the proportions of individual genotypes
among children presenting with non-SMA (n = 222) versus SMA (n = 165). Similarly, there was no associations between
the individual genotypes (−7402 T/G and -4729G/A) and SMA. Additional analyses, however, revealed that proportions of
individuals with -7402 T/-4729A (TA) haplotype was significantly higher in children presenting with SMA than non-SMA
group (P = 0.043). A further multivariate logistic regression analyses, controlling for confounding factors, demonstrated
that carriage of the TA haplotype was associated with increased susceptibility to SMA (OR; 1.564, 95% CI; 1.023-2.389,
P = 0.039). In addition, circulating levels of IL-13 were comparable between the clinical groups as well as across genotypes
and haplotypes. Collectively, findings presented here suggest that haplotypes within the IL-13 promoter at -7402 T/G
and -4729G/A may modulate SMA pathogenesis, but do not affect circulating IL-13 levels | en_US |
